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微小 RNA-143 在人膀胱癌 T24 细胞中作为肿瘤抑制因子发挥作用。

MicroRNA-143 functions as a tumor suppressor in human bladder cancer T24 cells.

机构信息

The United Graduate School of Veterinary Sciences, Gifu University, Yanagido, Gifu, Japan.

出版信息

Cancer Lett. 2011 Aug 28;307(2):211-20. doi: 10.1016/j.canlet.2011.04.005. Epub 2011 May 6.

DOI:10.1016/j.canlet.2011.04.005
PMID:21550168
Abstract

MicroRNA (miR)-143 and -145 were down-regulated in human bladder cancer T24 cells. The enforced expression of miR-143 induced growth-suppression in T24 cells through down-regulation of ERK5 and Akt expression at translational level, and chemically-modified synthetic miR-143 (miR-143/BP) exhibited a greater growth inhibitory effect than wild-type miR-143. In addition, the synthetic miR-143/BP induced apoptotic cell death in some of the transfected cells. Furthermore, co-treatment with the synthetic miR-143/BP and cisplatin showed the additive growth-suppressing effect on T24 cells. These findings suggest that the chemically-modified synthetic miR-143 functions as a tumor suppressor in T24 cells by targeting ERK5 and/or Akt.

摘要

微小 RNA(miR)-143 和 -145 在人膀胱癌 T24 细胞中下调。miR-143 的强制表达通过在翻译水平下调 ERK5 和 Akt 的表达来诱导 T24 细胞的生长抑制,并且化学修饰的合成 miR-143(miR-143/BP)表现出比野生型 miR-143 更强的生长抑制作用。此外,合成 miR-143/BP 在一些转染的细胞中诱导凋亡性细胞死亡。此外,合成 miR-143/BP 与顺铂联合治疗对 T24 细胞表现出相加的生长抑制作用。这些发现表明,化学修饰的合成 miR-143 通过靶向 ERK5 和/或 Akt 在 T24 细胞中作为肿瘤抑制剂发挥作用。

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